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EFFECT OF INTERFERON INDUCERS ON NK CELL CYTOTOXICITY

干扰素诱导剂对 NK 细胞毒性的影响

基本信息

批准号：
3169570
负责人：
EVA LOTZOVA
金额：
$ 16.53万
依托单位：
UNIVERSITY OF TX MD ANDERSON CAN CTR
依托单位国家：
美国
项目类别：
财政年份：
1982
资助国家：
美国
起止时间：
1982-02-01 至 1987-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3169570
关键词：
B lymphocyte T lymphocyte biological models cell mediated cytotoxicity cellular oncology fibrosarcoma immunotoxicity interferon inducers interferons lymphoma metastasis myelogenous leukemia neoplasm /cancer immunology neoplasm /cancer immunotherapy

项目摘要

There is increasing evidence that natural killer (NK) cells may play an important role in resistance against growth of tumors in vivo. However, most of the studies on NK cell-mediated cytotoxicity have focused on in vitro studies, and only a limited number of investigations concerning NK cells in vivo antitumor potential have been done. The aim of our studies was to investigate involvement of NK cells in in vivo resistance to murine tumors. Using murine ascitic mammary adenocarcinoma 755 model, we found a correlation between augmentation of NK cell cytotoxicity and resistance to the growth of 755 tumor. Specifically, NK cell inducer of pyrimidinone group, 2-amino-5-iodo-6-phenyl-4 pyrimidinol (AIPP), induced high levels of NK cell activity in peritoneal cavity concomitantly with high resistance of B6D2F1 mice to the growth of 755 tumor, the tumor that grew rapidly in control mice. Additionally, such tumor-protective effect was abrogated when the AIPP-stimulated mice were treated with NK cell-specific antiserum NK.1 but not with T-cell-directed antiserum Thy 1.2. These experiments suggest that NK cells are involved in resistance to mammary adenocarcinoma 755 and suggest that AIPP may be a useful therapeutic agent. The studies on the mechanism of NK cell augmentation indicate that both NK cell tumor-binding, as well as tumor lytic capacity, was augmented by AIPP and that such augmentation was mediated by regionally induced interferon. (HF)

越来越多的证据表明，自然杀伤(NK)细胞可能在在抵抗体内肿瘤生长方面发挥重要作用。然而，目前对NK细胞介导的细胞毒作用的研究主要集中在体外研究，以及关于NK的有限数量的研究细胞在体内的抗肿瘤潜能已经做好了。我们研究的目的是目的是探讨NK细胞在小鼠体内耐药中的作用肿瘤。利用小鼠腹水型乳腺癌755模型，我们发现 NK细胞杀伤活性增强与耐药的相关性 755肿瘤的生长情况。具体地说，嘧啶酮的NK细胞诱导剂组，2-氨基-5-碘-6-苯基-4-嘧啶醇(AIPP)，诱导高水平的腹膜腔内NK细胞活性与高抗药性 B6D2F1小鼠对755肿瘤的生长，该肿瘤生长迅速控制小鼠。此外，这种肿瘤保护作用也被取消了。用NK细胞特异性抗血清治疗AIPP刺激的小鼠 NK.1，但不能与T细胞定向的抗血清Thy 1.2结合。这些实验提示NK细胞参与了乳腺癌的耐药 755，提示AIPP可能是一种有用的治疗剂。这些研究关于NK细胞增强机制的研究表明，NK细胞 AIPP和AIPP增强了肿瘤结合和肿瘤裂解能力这种增强是由局部诱导的干扰素介导的。(Hf)